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Boards and Wards Complete > Heme Onc + Surgery Part 1 (111-156) > Flashcards

Heme Onc + Surgery Part 1 (111-156) Flashcards

1
Q

Endometriosis within uterine wall

A

Adenomyosis

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2
Q

Endometriosis within ovary

A

Endometrioma

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3
Q

What is the MCV of a microcytic anemia?

A
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4
Q

What 2 general reasons can there be for a decreased MCV

A
  1. decreased HB production

2. Impaired Hb function

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5
Q

If you’ve determined that pt has Iron deficiency anemia, whats the NEXT STEP

A

figure out why iron deficient

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6
Q

Whats the number 1 anemia in the world?

A

Iron deficiency

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7
Q

What’s the number one cause of iron deficiency in the world?

A

Hookworms

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8
Q

What population often has increased incidence of Iron deficiency?

A

Women of childbearing age secondary to menses

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9
Q

Dx in elderly with iron deficiency

A

Colon cancer until proven otherwise

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10
Q

What population has dietary iron deficiency?

A

Children, basically impossible in adults.

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11
Q

Reason out why pt with iron deficiency would have following sx:

  • tachycardia
  • fatigue
  • pallor
  • smooth tongue
  • brittle nails
  • esophagel webs
  • pica
A

not sure about smooth tongue

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12
Q

In Iron deficiency anemia ___ serum iron ___TIBC

A

decreased serum iron

increased TIBC

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13
Q

What is on peripheral smear for iron deficiency anemia?

A

Target cells

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14
Q

Tx for iron deficiency? Tx goal?

A

iron sulfate - should reach baseline hematocrit within 2 months

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15
Q

Ineffective erythropoiesis because of disorder of porphyrin pathway. Dx?

A

Sideroblastic anemia

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16
Q

What are 3 causes for sideroblastic anemia?

A

Chronic alcoholism
Drugs (INH)
Genetic

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17
Q

What do the labs for sideroblastic anemia look like?
___ iron
___TIBC
___ ferritin

A

Increased Iron
N/Increased TIBC
increased ferritin

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18
Q

What cells are seen with sideroblastic anemia

A

Ringed sideroblasts

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19
Q

Tx for sideroblastic anemia

A

Pyridoxine (B6)

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20
Q

Pt with anemia, encephalopathy (worse in children), seizures, ataxic gait, WRIST/FOOT DROPS, Dx?

A

Lead poisoning

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21
Q

What are Bruton’s lines?

A

Blue gray discoloration seen at gumlines in lead poisoning.

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22
Q

What is the classic finding of cells in lead poisoning?

A

basophilic stippling of RBC

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23
Q

What is the xray finding of lead posisoning?

A

Lead lines and increased density at the metaphyses of long bones

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24
Q

Tx of lead poisoning

A

chelation therapy with dimercaprol (BAL) and or ethylene diaminetetraacetic acid (EDTA)

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25
Q

Hereditary disease of decreased production of globin chains causing decreased Hb

A

Thalassemias

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26
Q

How do we differentiate the various thalassemias?

A

Gel electrophoresis of globin proteins

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27
Q

Whats the mechanism of alpha thalassemia?

A

decreased production of alpha globin chains (4 alleles)

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28
Q

What are the 3 most common (in decreasing order) of populations that get thalassemia?

A

.1 Asian

  1. African
  2. Mediterranean
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29
Q

If 4 alpha alleles are affected, what dz occurs?Blood smear?

A

hydrops fetalis
fetal demise/total body edema
smear Barts gamma4 Hb

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30
Q

If 3 alpha alleles are affected, what dz occurs?Blood smear?

A

HbH disease
Precipitation of B chain tetramers
Intraerythrocyte inclusions

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31
Q

If 2 alpha alleles are affected, what dz occurs?Blood smear?

A

Alpha thalassemia minor
Clinically silent
Mild microcytic anemic

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32
Q

If 1 alpha allele is affected, what dz occurs?Blood smear?

A

Carrier state
No anemia - asymptomatic
Blood smear not abnormal

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33
Q

In beta thalassemia, what 2 populations are most affected?

A
  1. Mediterranean

2. African

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34
Q

Pt starts developing anemia at age 6mo and has splenomegaly, frontal bossing, iron overload

A

Thalassemia major

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35
Q

How do you dx thalassemia?

A

Elecrophoresis

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36
Q

Why does frontal bossing occur in Beta thalassemia?

A

secondary to extramedullary hematopoiesis

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37
Q

Why does iron overload occur in beta thalessemia?

A

secondary to transfusions.

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38
Q

What are the lab findings for beta thalassemia?

HbA? HbA2? HbF?

A

Very decreased HbA
increased HbA2
Increased HbF

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39
Q

What is the treatment for thalassemia major?

A
  • Folate
  • splenectomy if splenomegaly
  • transfuse if severe anemia
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40
Q

How does B-thalassemia minor present? Lab findings, Tx?

A

Asymptomatic
Electrophoresis (same findings as major)
Tx by avoiding oxitative stress

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41
Q

What happens to HbS in sickle cell anemia?

A

HbS tertramer polymerizes causing sickling deoxygenated RBCs

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42
Q

Why does vaso-occlusion occur in Sickle cell pts?

A

Bc blood isn’t carrying enough O2, vasoconstriction occurs causing sickled cells to get trapped –> pain crisis.

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43
Q

What signs/sx occur because of vaso-oclusion

A

pain crisis, myocardiopathy

infarcts of bone/CNS/lungs/kidneys and auto-splenectomy

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44
Q

What are sickle cell patients more succeptible to because of autosplenectomy?

A

Encapsulated bacteria

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45
Q

Failure of all types of blood cell growth (aplastic anemia) occurs in sickle cell pts because of what virus?

A

Parvo virus B19

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46
Q

When intravascular hemolysis occurs in sickle cell patients, what is one complication they can develop esp children and teens

A

Gall stones

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47
Q

What is the treatment for sickle cell?

A

O2 – transfusion as needed
Hydroxyurea to decrease the incidence and severity of pain crisis
Pneumococcal vaccine bc of increased risk of infection.

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48
Q

What is the MCV for megaloblastic anemia?

A

> 100

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49
Q

Why do megaloblastic anemias occur?

A

decreased DNA synthesis with normal RNA/protein synthesis

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50
Q

What does the blood smear for megaloblastic anemia look like?

A

hypersegmented neutrophils

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51
Q

What is the most common cause of B12 deficiency?

A

pernicious anemia

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52
Q

What is the mechanism of pernicious anemia?

A

Antibodies to gastric parietral cells which decreases intrinsic factor (needed for B12 uptake in the terminal ileum)

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53
Q

Why does atrophic gastritis occur with pernicious anemia?

A

Anti-parietal Abs attack parietal cells –> inflammation to stomach mucosa –> grandular tissue is replaced by fibrous tissue –> achlorydia (decreased HCl production)

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54
Q

Name 2 other causes of B12 deficiency?

A

Resection of terminal ileum or diphyllobothrium latum infection.

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55
Q

B12 deficiency causes what signs/sx in blood? neuro?

A

megaloblastic anemia

neuro signs = peripheral neuropathy, parasthesias, WORSE IN LEGS

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56
Q 
What are the diagnostic lab findings of B12 deficiency?
\_\_\_ Mehtylmalonic acid
\_\_\_ Homocystiene 
\_\_\_ B12
\_\_\_ MCV
A

increased MMA
Increased Homocysteine (more sensitive than b12 level)
Decreased B12
>100 MCV.

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57
Q

Tx for B12 deficiency?

A

High dose b12 (oral proven to be equivalent to parenteral)

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58
Q

Where is folic acid derived from?

A

green, leafy vegetables (foliage)

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59
Q

What is the most common reason for folate deficiency?

A

dietary

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60
Q

What two states of the human body increase folate requirement?

A

Pregnancy or hemolytic anemia

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61
Q

What two drugs inhibit folate reduction into tetrahydrofolate?

A

Methotrexate and prolonged TMP-SMX

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62
Q

What symptoms does folic acid deficiency manifest?

A

Megaloblastic anemia, no neuro signs (unlike B12)

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63
Q

Labs for folic acid deficiency?
___ Methylmalonic acid
___ Homocysteine
___ Folate

A

Normal MMA
Increased homocysteine (more sensitive than folate levels)
May or may not be decreased folate

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64
Q

Treatment for folic acid deficiency?

A

Folic acid oral supplementation

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65
Q

What is a normocytic anemia MCV?

A

between 80 and 100

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66
Q

What two categories of normocytic anemia divided into?

A

hypoproliferative and hemolytic

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67
Q

What are the 3 normocytic hypoproliferative anemias?

A

Anemia of renal failure
Anemia of chronic disease
Aplastic anemia

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68
Q

What is the mechanism behind anemia of renal failure?

A

EPO production is decreased by kidney in chronic renal failure

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69
Q

How do you treat anemia of renal failure?

A

EPO

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70
Q

What is the mechanism behind anemia of chronic disease?

A

Chronic inflammation states like (cancer, TB, fungal, infxn or collagen vascular disease) cause release of hepcidin from the liver as an acute phase reactant so iron is inhibited from gut absorption.

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71
Q

What labs can help diagnose anemia of chronic disease?
___Serum iron
___ferritin
___ TIBC

A

decreased serum iron
normal/increased territin
decreased TIBC

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72
Q

What is the mechanism behind aplastic anemia?

A

Bone marrow failure, usually idiopathic, parvovirus B19, hepatitis virus, radiation, drugs like chloramphenicol

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73
Q

How do you dx aplastic anemia? What will bone marrow biopsy show?

A

Bone marrow biopsy will show hypocellular marrow

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74
Q

What are the 4 ways to get hemolytic anemia?

A

Spherocytosis
Auto immune hemolysis (IgG mediated)
Cold agglutinin disease (IgM mediated)
Mechanical destruction

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75
Q

What is the mechanism of spherocytosis?

A

Autosomal dominant defect in spectrin causes stiff RBCs to be trapped in the spleen

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76
Q

What does spherocytosis present with in childhood?

A

Childhood jaundice and gall stones

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77
Q

Which type of bilirubin is elevated in spherocytosis?

A

Indirect hyperbilirubinemia

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78
Q

Is spherocytosis Coombs + or -

A

negative Coombs

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79
Q

What does the peripheral smear for spherocytosis show?

A

Spherocytes

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80
Q

What is the treatment of spherocytosis?

A

Folic acid and splenectomy for severe disease

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81
Q

What is the most common and other causes for autoimmune hemolytic anemia?

A

Idiopathic (MC)

lupus, drugs, leukemia, lymphotma (others)

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82
Q

Signs and sx of autoimmune helomlytic anemia?

A

Rapid onset, spherocytes on blood smear

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83
Q

Labs seen for autoimmune hemolytic anemia?
____ indirect bilirunin
____ haptoglobin
____urine hemosierin

A

increased indierct bilirubin
decreased haptoglobin
increased urine hemosiderin.

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84
Q

What is the definitive diagnosis for hemolytic anemias?

A

direct coombs test positive

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85
Q

What is the 1st, 2nd and 3rd line treatment for hemolytic anemia?

A

1st give prednisone

  1. Rituximab (anti-CD20 B cell Mab)
  2. splenectomy.
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86
Q

What is the most commonly idiopathic anemia that could also result from Mycoplasma pneumoniae or Mono (CMV or EBV)

A

Cold-agglutinin disease (IgM mediated. )

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87
Q

Pt gets anemia s/p cold or uri. Dx?

A

Cold agglutinin disease

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88
Q

Dx test for cold agglutinin disease

A

cold agglutinin test or direct coombs test

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89
Q

Tx for cold agglutinin disease

A

Prednisone, supportive

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90
Q

What are the causes of mechanical destruction of RBCs? (4)

A

DIC, TTp, HUS and artificial heart valve

91
Q

What would be seen on peripheral smear for mechanical destruction?

A

Schistocytes

92
Q

At what platelet amount does bleeding time increase?

A

less than 50,000

93
Q

At what platelet amount does clinically significant bleeding start?

A

less than 20,000

94
Q

At what platelet amount do CNS bleeds start to occur?

A

less than 10,000

95
Q

What are some causes of thrombocytopenia? (5)

A

ITP, TTP, HUS, DIC, Drug induced.

96
Q

How does ITP differ in children and adults?

A

ITP is auto-antibody mediates platelet destruction. In children it occurs after URI and is self-limiting. In adults, its chronic.

97
Q

Whats the treatment for ITP

A

Steroids, IVIG –> splenectomy –> rituximab (anti CD20) for refractory disease.

98
Q 
Hemolytic anemia
Thrombocytopenia
Renal failure
Fever
Neurologic disease
is the pentad for what disease?
A

Throbotic thrombocytopenic purpupa (TTP) - often idiopathic and seen in HIV, fatal.

99
Q

What is the Tx for TTP

A

Tx: Plasma exchange

100
Q

Kid presents with ARF, bloody diarrhea, abd pain, seizures, FULMINANT THROMBOCYTOPENIA w HEMOLYTIC ANEMIA

A

Hemolytic uremic syndrome (HUS) often bc Ecoli 0157:H7

101
Q

What is the tx for HUS?

102
Q

What are some drugs that can induce thrombocytopenia?

A

Heparin, sulfonamides, valproic acid –> reversible if agent is stopped

103
Q

What is the most common inherited hypercoagulable disorder?

A

vWF deficiency (although some places say Factor V)

104
Q

vWF deficiency shows what labs? PT/PTT? BT?

A

Episodic increased BT

Normal PT/PTT

105
Q

How do you diagnose vWF?

A

vWF levels and ristocetin-cofactor test

106
Q

What is the Tx for VWF deficiency? Tx for active bleed?

A

DDAVP which increased vWF secretion
OR
Cryoprecipitate for active bleed

107
Q

X-linked deficiency of factor VIII

A

Hemophilia A

108
Q

X- linked deficiency of factor IX

A

Hemophilia B (aka Christmas disease)

109
Q

What is the major sign/sx for hemophilia?

Labs? PT/PTT/BT?

A

bleeding into a joint (hemarthroses)
Increased PTT
normal PT
Normal BT

110
Q

What is the Tx for hemophilia?

A

Give recombinant Factor VIII or IX concentrate

111
Q

What are 3 myeloproliferative disorders?

A

Polycythemia vera
Essential thrombocythemia
Idiopathic myelofibrosis

112
Q

What causes myeloproliferative diseases?

A

Clonal proliferation of myeloid stem cell –> leads to excessive production of mature differentiated myeloid cell lines

113
Q

What is the danger of myelopriliferative diseases?

A

They can all transform into acute leukemias

114
Q

Pt is a 50-60 yr old MALE with HA, diplopia, retinal hemorrhages, claudication, early satiety, splenomegaly, gout, PRURITIS AFTER SHOWERING, BASOPHILIA

A

Polycythemia vera

115
Q

Tx for polycythemia vevra

A

phlebotomy and hydroxyurea

116
Q

Pt with platelet count >1x10^6, splenomegaly and ecchymosis. All other causes like iron deficiency and malignancy were r/o. Dx?

A

Essential thrombocythemia

117
Q

Tx for essential thrombocythemia?

A

anagrelide and plateletpharesis

118
Q

Pt >50 yrs old with MASSIVE hepatosplenomemgaly and TEARDROP cells on peripheral smear. Dx?

A

Idiopathic myelofibrosis

119
Q

What is the prognosis for idiopathic myelofibrosis? What does it progress to?

120
Q

What situations can secondary thrombocytosis be seen? Counts often >1 million

A

Any chronic inflammatory disorder like infxn, bleed, iron deficiency anemia or following splenectomy.

121
Q

What is the most common neoplasm in children (peak age 3-4)

122
Q

What peripheral blood blasts are seen positive in ALL?

A

PAS+
CALLA +
TdT +

123
Q

What is the prognosis for cure of ALL in children?

A

Good, 80%. Much worse in adults.

124
Q

What is the most common leukemia in adults?

125
Q

What blasts are + in blood for AML?

A

MPO+
Sudan Black +
Auer Rods +

126
Q

What is the Tx for the M3 subtype of AML?

A

All-trans retinoic acid

127
Q

What complication must we be especially careful about in AML?

128
Q

Which leukemia presents most commonly in >50yrs old and can result in BLAST crisis within 3-6 mos… though the onset is about 3-4 years?

129
Q

What chromosome is + in serum for CML?

A

Philadelphia chromosome

130
Q

What is different about the cells in the peripheral blood and what interesting marker does it have?

A

Peripheral blood has cells of all maturational stages.

Also, decrease in leukocyte alkaline phosphatase.

131
Q

What translocation is the PHL chromosome?

A

abl gene on chromosome 9 to bcr on chromosome 22

132
Q

Tx for CML

A

Tyrosine kinase inhibitor like imatinib seylate. If fails, BMT can be curative

133
Q

Pt had this asymptomatic cancer for many years and only recently started to present with organomegaly, thrombocytopenia, hemolytic anemia. Morphology of blood and marrow smear are normal.Tx?

A

CLL

Tx: palliative, early tx doesnt prolong life.

134
Q

Which leukemia has a characteristic hairy cell morphology and pancytopenia? Tx?

A

B cell subtype of hairy cell leukemia

Tx: INFalpha and splenectomy

135
Q

What type of leukemias generally involve skin and present with erythematous rashes?

A

T cell leukemias

136
Q 
MC leukemias by age
15
15-39
40-59
>60
A

15 ALL
15-39 AML
40-59 AMLand CML
>60 CLL

137
Q

Teenage presents with a cancer in head and neck

A

Non hodgkins lymphoma

138
Q

Which lymphoma is closely related to EBV?

A

Burkitt’s lymphoma

139
Q

African Burkitt’s involves which body parts?

US Burkitts?

A

African - starry sky

US- abdomen

140
Q

What’s seen on pathology for Burkitts?

A

Starry sky - spaces scattered within densely packed lymph tissue

141
Q

What is typical therapy for Non Hodgekins?

A 
R-CHOP
Rituximab
Cyclophosphamide
Hydroxydaunarrubacine (Adrimycin)
Oncovin (vincristine)
Prednisone
142
Q

Elderly pt comes in with diffuse scaly rash or erythroderma (total body erythema). Path report shows stained cells with ceribriform nuclei (cerebral gyri)

A

Cutaneous T cell lymphoma (CTCL)

Leukemic phase called Sezary syndrome

143
Q

Treatment of CTCL?

144
Q

Pt with nasal T cell lymphoma (lethal midline granuloma) and pulmonary angiocentric lymphoma . Large mass, biopsy just shows diffuse necrosis. Tx?

A

Angiocentric T cell lymphoma

Tx: palliative radiation, prognosis poor

145
Q

What population does Hodgkins lymphma affect?

A

Bimodal age distribution, young men and elderly

146
Q

What concurrent infection is present in 50% of cases of Hodgkins?

147
Q

What type of fevers are present in Hodgkins?

A

Pel-Ebstein (fevers wax and wane)

148
Q

Pt has Pel-ebstein fevers, chills, night sweats, weight loss, pruritis. What makes these symptoms worse?

A

Alcohol intake worsens Hodgkins lymphoma sx.

149
Q

What cells are visible on path for Hodgkins

A

Reed-Stern berg Owl eyes. Binucleated Giant Cells or Mononucleated Giant Cell.

150
Q

What defines each stage of cancer?

A

Stage 1 = 1 lymph node involvement –> radiation
Stage 2 = >2 lymph nodes involved on same side of diaphragm –> radiation
Stage 3 = Involvement on both sides of diaphragm –> chemo
Stage 4 = disseminated to organs or extranodal tissue–> chemo

151
Q

What are 2 chemotherapy regimens?

A 
MOPP = mechlorethamine, Oncovin, Procarbazine, prednisone
ABVD = adriamycin, belomycin, vincristine, dicarbazine.
152
Q

For urgent K+ repletion, what to give at what rates?

A

Give IV 10 mEq/h through peripheral line of 20 mEq/hr through central line
Give oral K simultaneously at upto 40 mEq/hr

153
Q

If you replete K+ too quickly, what is the side effect?

A

vessel necrosis

154
Q

By how much does each 10 mEq oral or IV increase the total serum K in the body?

A

Increases serum K by 0.1 mmol/L

155
Q

Peri-MI, K level should be kept above ___ to suppress arrhythmia- be aggressive

156
Q

What is the sequence of EKG changes for hyperkalemia?

A
  1. Peaked T waves
  2. Diminished R waves
  3. Widening of QRS
  4. Prolonged PR interval
  5. Loss of P wave
  6. Sine wave.
    look on page 135 for reference.
157
Q

To treat emergent hyperkalemia, why do we give IV calcium gluconate? What do we follow this with?

A

IV calcium gluconate given to stabilize myocardial cell membranes –> this does not lower potassium.

We then give Glucose + Insulin which will lower the plasma potassium for several hours.
This can be given +/- Kayexalate oral or per rectum to drop K levels for 24 hrs.

158
Q

How much of our lean body weight is water? Where in body is it?

A

50-70% mostly located in skeletal muscle

159
Q

What fraction of total body water is intracellular and extracecllular?

A

Intracellular (2/3)

Extracecllular (1/3)

160
Q

What is the 3 for 1 rule of Fluid management?

A

Since only 300mL of a 1L lactate ringer solution stays intravascularly, you should replete 3 to 4 times the vascular defecit.

161
Q

In what patients are colloid solutions most useful?

A

edematous patients because colloid solutions have high molecular weight and stay intravascular for longer

162
Q

What complication could starch solutions have?

A

Increased tissue accumulation leading to coagulopathy and renal failure.

163
Q

How much fluid does an uncomplicated patient NPO lose per day?

A

> 1 L of fluid from sweat, urine, feces and respiration.

164
Q

How do you know if you are adequately rehydrating a patient?

A

Urine output > 0.5 cc/kg/hr (for typical patient 30 cc/hr)

165
Q

What is the number 1 cause in inpatients for hypercalcemia?

A

Malignancy involving bone, parathyroid or kidney

166
Q

What physical exam sign would you see in patients with hypocaclcemia?

A

Chvostek’sand Trousseau signs

167
Q

What electrolyte disorder would Cushing’s often cause?

A

Hypokalemia

168
Q

What electrolyte disturbance would refeeding syndrome cause?

A

Hypophosphatemia

169
Q

Explain cascade of thrombus formation starting from endothelial damage?

A

Endothelial damage –> platelets bind to subendothelium through interaction of von Willebrand factor –> platelets release ADP, 5HT, and platelet derived growth factor –> platelets bind to eachother via GP2b-3a forming thrombus

170
Q

Review Coagulation cascade

A

Review coagulation cascade

171
Q

Where is vitamin K derived from?

A

leafy vegetables and colonic flora

172
Q

Which cofactors need vitamin K for gamma-carboxylation

A

2 7 9 10 factors C and S

173
Q

When is pre-operative lab screening warrented?

A

Only if there are signs and sx suggestive of underlying bleeding disorder

174
Q

1 unit of packed RBC should raise Hb and hematocrit by how much?

A

1 g/dL Hb and 3% Hct

175
Q

What is the most common cause of acute rejection of blood products?

A

clerical error

176
Q

What should be done in case of acute rejection of blood?

A

stop transfusion and administer IV fluids to maintain urine output.

177
Q

Which hepatitis are you most likely to be at risk for with prior hx of blood transfusion?

A

Hepatits C

178
Q

What level should platelets be transfused to?

A

maintain at 50,000 because significant bleeding does not occur unless lower than that

179
Q

What is the most common complication of platelet transfusion?

A

alloimmunization –> platelet counts continue to fall despite continued transfusion.

180
Q

Why might platelet alloimmunization occur?

A

Antibodies to donor’s MHC (major histocompatibility complex)

181
Q

How to treat pt if platelet alloimmunization is occuring?

A

Single donor HLA matched platelets

182
Q

Which blood product contains all coagulation factors?

A

Fresh frozen plasma

183
Q

What is cryoprecipitate rich in?

A

Factor VIII, fibrinogen and fibronectin.

184
Q

If a uremic patient is having severe bleeding secondary to platelet dysfunction, what to treat with?

A

DDAVP or cryoprecipitate…. NEVER TRANSFUSE MORE PLATELETS –> they’ll just become dysfunctional too

185
Q

How long prior to surgery should asprin be discontinued?

186
Q

What is the most common post operative cardiac event?

A

Atrial fibrillation

187
Q

What is the most important factor to consider to see if pt is at risk for pulmonary complications post op?

A

If pt has hx of COPD

188
Q

Azotemia, sepsis, intraoperative hypotension, nephrotoxic drugs and radiocontrast agents all put patient at risk for what?

A

post operative renal failure

189
Q

What measures can be taken to avoid contrast associated nephropathy (CAN)?

A

Expand intravascular volume with IV fluids and using N acetyl cysteine or sodium bicarbonate prior to administering radiocontrast dye.

190
Q

What preventative measure must you take pre-op for all pts with prosthetic heart valves?

A

Give antibiotic prophylaxis to prevent bacterial endocarditis

191
Q

What should always be on the differential of post op dyspnea?

A

Pulmonary embolus

192
Q

What precaution must be taken for patients on corticosteroids >1 wk preoperatively and with any pt with primary adrenal insufficiency?

A

Give steroid replacement via hydrocortison before, during and after surgery to approximate response of normal adrenal gland ..

Normal surgical response is to secrete corticosteroids but this response is diminished in pts taking steroids or if they have adrenal insuff.

193
Q

Pt s/p operation has unexplained hypotension and tachycardia despite fluid and vasopressor administration. Tx?

A

Pt is in adrenal crisis. Give corticosteroids which will dramatically improve BP

194
Q

What is the differential for post op fever in order of post op days?

A 
Wind (lungs)
Water (urinary tract)
Wound
Walking (DVT)
Wonder drug (drug reaction)
195
Q

What anesthetics trigger malignant hyperthermia? Tx?

A

halothane, isoflurane, succinylcholine

Treat with dantrolene, cooling measures and ICU monitoring

196
Q

What is the MCC of death in pts

197
Q

When surveying the airway, if it cannot be established, what should you do? What do unconscious patients need?

A
  • Use large bore 14 gauge needle insert it into the cricothyroid membrane
  • Unconscious pts need endotracheal intubation
198
Q

What does the cxray look like for a tension pneumothorax? Sx? Tx?

A

contralateral mediastinal shift along with distended neck veins due to increased CVP. Also will have hypotension, absent breath sounds and hyperresonance to percussion on affected side.

Tx: Immediate chest tube or 14 gauge needle puncture of affected side.

199
Q

What is a flail chest a result of? Tx?

A

Multiple rib fractures, tx: intubation with mechanical ventillation

200
Q

Injury to the great vessels causes what?

A

massive hemothorax requires chest tube

201
Q

Neck trauma can occur in 3 zones. What imaging is used to assess neck trauma?

A

look at pic on 150. Use 4 vessel angiography

202
Q

What kind of needles are put in to maintain circulation?

A

Two large-bore IV placed in upper extremities. For severe shock, place central venous line

203
Q

What is the indication for a FAST exam?

A

intraperitoneal hemorrhage or pericardial tamponade
History of abdominal trauma, hypotensive or unable to provide a reliable history because of impaired consciousness due to head injury or drugs.

204
Q

What are the 4 areas assessed with a FAST exam?

A
  1. Periherpatic (hepatorenal space)
  2. Perisplenic
  3. Pelvis
  4. Pericardium
205
Q

What is the DDx for loss of consciousness?

A 
Alcohol
Epilepsy
Insulin
Overdose
Uremia

Trauma
Infection
Psychogenic
Stroke

206
Q

What is the Tx for LOC in an emergent situation where cause is unknown

A

Tx: coma cocktail –> dextrose, thiamine naloxone and O2

207
Q

What is Cushing’s triad?

A

HTN, bradycardia and bradypnea seen when there is increased ICP

208
Q

Tx for Pt with “Disability” including Cushings triad and increased ICP?

A

Ventillation to keep PaCO2 at 30-40 mm Hg, control fever, administer mannitol, corticosteroids and even bony decompression if needed

209
Q

What does ABCDE stand for in trauma situations?

A 
Airway
Breathing
Circulation
Disability
Exposure
210
Q

What do racoon eyes and Battle’s sign indicate?

A

Periorbital and mastoid hematomas

211
Q

If blood is noted at the urethra, what must be done before placing a bladder catheter?

A

retrograde urethrogram

212
Q

What is hematuria s/p trauma suggest?

A

significant retroperitoneal injury

213
Q

What happens to the pulmonary capillary wedge pressure in cardiogenic shock?

A

increased PCWP

214
Q

What is the treatment for compartment syndrome?

A

Fasciotomy

215
Q

What is the defect and tx for hypovolemic shock?

A

decreased preload – 2 large bore IVs with crystalloid infusions 3 for 1 rule

216
Q

What is the defect and tx for cardiogenic shock?

A

Myocradial failure – Pressors dobutamine is first line

217
Q

What is the defect and tx for septic shock?

A

Decreased peripheral vascular resistance – Give norepinephrine to vasoconstrict peripheral arterioles to prevent multiple organ dysfunction syndrome (MODS)

218
Q 
Which layer of dermis do the following burns affect?
1st deg
2nd deg
3rd deg
4th deg
A

1st deg superficial dermis
2nd deg epidermis
3rd deg skin and subQ tissue
4th deg affects muscle and bone

219
Q

How do you calculate the percentage of Body surface affected? (BSA)

A

See image on p 155

220
Q

How do you calculate and administer fluid resuscitation to a burn victim? How is it given?

A

Parkland fomula = %BSA * weight (kg) * 4
Used to calculate amount of crystalloid needed

Give half of fluid in the first 8 hours and give the remainder over the next 16 hours

221
Q

Why is it important to make burn patient NPO?

A

must have return of bowel function

222
Q

What are the nutritional requirements of a burn pt?

A

High protein and caloric requirements with vitamin supplementation.

223
Q

What is a Marjolin’s ulcer?

A

squamous cell carcinoma arisng from an ulcer or burn

224
Q

What is a Curling’s ulcer?

A

acute duodenal ulcer seen in burn patients

Boards and Wards Complete (13 decks)

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